The proposed work is intended to define whether the central hypertensive effect and hydration changes produced by angiotensin are related to extracellular sodium concentration. The specific experiments planned include the following. 1. The methodology to record CSF (Na ion) in conscious rabbits (now developed) will be employed to determine whether hypovolemic conditions raise CSF (Na ion) and if this correlates with water intake, plasma vasopressin and plasma renin activity. This work will assess whether osmotic and volume mechanisms regulating hydration share in common a sodium dependent mechanism. 2. The effects of i.v. angiotensin on (Na ion) and Na22 movement into CSF of conscious rats will be ascertained in normal, hypovolemic and cellular dehydration conditions. These experiments will determine if peripheral angiotensin alters hydration by facilitating sodium entry into brain. 3. Conscious rats will be centrally infused for 5 days with antiangiotensin II serum, vasopressin antiserum on equivalent amounts of normal serum. Water and food intakes will be recorded and terminal blood chemistries including hematocrit, (Na ion), (K ion), mOsm/kg, PRA, and vasopressin will be obtained. These experiments will determine whether removal of angiotensin and vasopressin activities from peri-ventricular structures affects body hydration. These goals for this fiscal year will establish (1) whether angiotensin activity in brain normally participates in the regulation of hydration and (2) whether changes in sodium movement is the mechanism of action. These data should allow further assessment of the potential role of angiotensin in the central nervous system in diseases of salt/water disturbances and hypertension. BIBLIOGRAPHIC REFERENCE: Severs, W.B., Drinking Behavior Produced by Angiotensin. in: Int. Cong. Endocrinology, 5th, Hamburg, 1976, V. James, ed., Endocrinology; Proceedings, Excerpta Medica, Amsterdam, in press.